Macrovolt T-Wave Alternans: Pathophysiology and Link With Repolarization Dispersion

Abstract

One of the earliest electrophysiologic signs of myocardial ischemia is alternation of the T-wave in duration and magnitude from beat to beat. Although ischemia-induced T-wave alternans (TWA) has been reported previously in clinical (1) and experimental settings (2), this phenomenon recently has achieved particular significance through the demonstration that TWA is a powerful predictor of ventricular fibrillation (3,4). Because the electrocardiographic T-wave is the body surface reflection of spatial and temporal differences in ventricular repolarization, a meaningful pathophysiological approach to T-wave alternans needs to address the electrophysiological mechanisms at the myocardial tissue level, specifically abnormalities of the action potential duration (APD) response. This approach will also help to understand why ischemic T-wave alternans increases dispersion of repolarization and facilitates ventricular tachyarrhythmias (VTA). The concept that APD-alternans sets up the conditions for VTA is based on the existence of different APDs in adjacent myocardial regions which result in substantial inhomogeneities of cellular repolarization. Such differences in APD could induce regional conduction block due to regionally disparate refractoriness or result in flow of injury current, both of which may facilitate VTA (5,6).